Mechanism and Regulatory Function of CpG Signaling via Scavenger Receptor B1 in Primary B Cells

摘要: It is well established that CpG promotes pro-inflammatory cytokine and antibody production by B cells via the Toll-like receptor 9 (TLR9)-dependent pathway. However, scavenger receptors (SRs) are also capable of binding such pathogen-derived molecules, yet their contribution to CpG-induced signaling events has not been evaluated. Here we identified a novel TLR9-independent mechanism immune function mediated B1 (SR-B1). Specifically, show CpG/SR-B1 triggers calcium entry into primary lymphocytes phospholipase Cγ-1-mediated activation TRPC3 channels cell adhesion vascular molecule-1. signals molecule-1 exclusively SR-B1. Although Ig induced require TLR9 expression, found SR-B1 negatively regulates TLR9-dependent interleukin-6, interleukin-10, IgM. Thus, our results provide perspective on complexity within demonstrating an alternative pathway for nucleic acid-induced provides feedback inhibition specific responses cells. Consequently, these have wide implications understanding mechanisms regulating tolerance acids pathogen-associated molecules.